The rheumatological system

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Chapter 9 The rheumatological system

Rheumatology is ‘the study of the Rheumatic Diseases including arthritis, rheumatic fever, fibrositis, neuralgia, myositis, bursitis, gout and other conditions producing somatic pain, stiffness and soreness’ (Oxford English Dictionary, 2nd edn, 1989). The rheumatological system therefore includes diseases of the joints, tendons and muscles.

The rheumatological history

Presenting symptoms (Table 9.1)

It is often useful to ask the patient to point to the painful place or area. For example, pain said to affect the knee may be in the popliteal fossa, the knee joint itself, or in the supra- or infra-patellar bursa. Remember also that pain in the knee or lower thigh may be referred from the hip (Figure 9.1).

Find out if the symptoms are of an acute or chronic nature and whether they are getting better or worse. The effect of rest and exercise on the joint pain should be determined. Patients with rheumatoid arthritis have joint symptoms which are worse after rest, while those with osteoarthritis have pain which is worse after exercise. Ask about the sequence of onset of joint involvement. Precipitating factors such as trauma should be noted. The causes of monoarthritis (single joint) and polyarthritis (more than one joint), and the patterns of polyarthritis in various diseases, are presented in Tables 9.2, 9.3 and 9.4.

TABLE 9.2 Causes of monoarthritis

A single hot red swollen joint (acute monoarthritis)

A single chronic inflamed joint (chronic monoarthritis)

TABLE 9.3 Causes of polyarthritis

TABLE 9.4 Patterns of polyarthropathy

Back pain

This is a very common symptom. It is most often a consequence of local musculoskeletal disease.

Ask where the pain is situated, whether it began suddenly or gradually, whether it is localised or diffuse, whether it radiates to the limbs or elsewhere, and whether the pain is aggravated by movement, coughing or straining. Musculoskeletal pain is characteristically well localised and is aggravated by movement. If there is a spinal nerve root irritation there may be pain that occurs in a dermatomal distribution. This helps to localise the level of the lesion. Diseases such as osteoporosis (with crush fractures), infiltration of carcinoma, leukaemia or myeloma may cause progressive and unremitting back pain, which is often worse at night (Table 9.6). The pain may be of sudden onset but is usually self-limiting if it results from the crush fracture of a vertebral body. In ankylosing spondylitis the pain is usually situated over the sacroiliac joints and lumbar spine, it is also worse at night and is associated with morning stiffness. The pain of ankylosing spondylitis is typically better with activity which helps distinguish it from mechanical back pain.1,2 Pain from diseases of the abdomen and chest (e.g. dissecting abdominal or thoracic aortic aneurysm) can also be referred to the back.

TABLE 9.6 Alarm features for back pain

Age > 50 years
Cancer history
Weight loss (unexplained)
Pain on waking from sleep
Pain for longer than one month and unresponsive to simple analgesics
Fever
History of drug use by injection
Bowel or bladder dysfunction

Limb pain

This can occur from disease of the musculoskeletal system, the skin, the vascular system or the nervous system.

Musculoskeletal pain may be due to trauma or inflammation. Muscle disease such as polymyositis can present with an aching pain in the proximal muscles around the shoulders and hips, associated with weakness. Pain and stiffness in the shoulders and hips in patients over the age of 50 years may be due to polymyalgia rheumatica. The acute or subacute onset of symptoms in multiple locations suggests an inflammatory process. Bone disease

TABLE 9.5 Functional assessment in rheumatoid arthritis

Class Assessment
Class 1 Normal functional ability
Class 2 Ability to carry out normal activities, despite discomfort or limited mobility of one or more joints
Class 3 Ability to perform only a few of the tasks of the normal occupation or of self-care
Class 4 Complete or almost complete incapacity with the patient confined to wheelchair or to bed

such as osteomyelitis, osteomalacia, osteoporosis or tumours can cause limb pain. Inflammation of tendons (tenosynovitis) can produce local pain over the affected area.

Vascular disease may also produce pain in the limbs. Acute arterial occlusion causes severe pain of sudden onset, often with coolness or pallor. Chronic peripheral vascular disease can result in calf pain on exercise that is relieved by rest. This is called intermittent claudication. Venous thrombosis can also cause diffuse aching pain in the legs associated with swelling.

Spinal stenosis can cause pseudo-claudication—pain on walking but relieved by leaning forward.

Nerve entrapment and neuropathy can both cause limb pain which is often associated with paraesthesiae or weakness. The usual cause is synovial thickening or joint subluxation—especially for patients with rheumatoid arthritis. The vasculitis associated with the inflammatory arthropathies can also cause neuropathy leading to diffuse peripheral neuropathy or mononeuritis multiplex. Patients with chronic rheumatoid arthritis often develop subluxation of the cervical spine at the atlanto-axial joint. This is caused by erosion of the transverse ligament around the posterior aspect of the odontoid process (dens). The patient may describe shooting paraesthesiae down the arms and an occipital headache. Neck flexion leads to indentation of the cord by the dens and can cause tetraplegia or sudden death. The abnormality may be obvious on lateral X-rays of the cervical spine (Figure 9.3). Injury to peripheral nerves can result in vasomotor changes and severe limb pain. This is called causalgia. Even following amputation of a limb, phantom limb pain may develop and persist as a chronic problem.

Dry eyes and mouth

Dry eyes and dry mouth are characteristic of Sjögren’s syndrome (Table 9.8). This syndrome may occur in isolation (primary Sjögren’s) and is very common in association with rheumatoid arthritis and other connective tissue disease. Mucus-secreting glands become infiltrated with lymphocytes and plasma cells, which cause atrophy and fibrosis. The dry eyes can result in conjunctivitis, keratitis and corneal ulcers. Sjögren’s syndrome can also have an effect on other organs such as the lungs or kidneys.

TABLE 9.8 Clinical features of Sjögren’s syndrome

In this syndrome mucus-secreting glands are infiltrated by lymphocytes and plasma cells, which cause atrophy and fibrosis of glandular tissue.
1 Dry eyes: conjunctivitis, keratitis, corneal ulcers (rarely vascularisation of the cornea)
2 Dry mouth
3 Chest: infection secondary to reduced mucus secretion or interstitial pneumonitis
4 Kidneys: renal tubular acidosis or nephrogenic diabetes insipidus
5 Genital tract: atrophic vaginitis
6 Pseudolymphoma: lymphadenopathy and splenomegaly, which may rarely progress to a true (usually non-Hodgkin’s) lymphoma

Note: This syndrome occurs in rheumatoid arthritis and with the connective tissue diseases.

Red eyes

The seronegative spondyloarthropathies and Behçet’sb syndrome but not rheumatoid arthritis may be complicated by iritis (eye pain with central scleral injection—a ‘red eye’—radiating out from the pupil) (see Figure 9.51, page 279). In other diseases, such as Sjögren’s, red eyes may be due to dryness, episcleritis or scleritis.

Past history

It is important to inquire about any history of trauma or surgery in the past. Similarly, a history of recent infection, including hepatitis, streptococcal pharyngitis, rubella, dysentery, gonorrhoea and tuberculosis, may be relevant to the onset of arthralgia or arthritis. A history of tick bite may indicate that the patient has Lyme disease. Inflammatory bowel disease can be associated with arthritis, as described on page 191. A history of psoriasis may indicate that the arthritis is due to psoriatic arthropathy. It is also important to inquire about any history of arthritis in childhood. The smoking history is important: rheumatoid arthritis is more common in smokers, and smoking adds to their already increased risk of cardiovascular disease.

The rheumatological examination

There are certain established ways of examining the joints and related structures3 and it is important to be aware of the numerous systemic complications of rheumatological diseases. The actual system of examination depends on the patient’s history and sometimes on the examiner noticing an abnormality on general inspection. Formal examination of all the joints is rarely part of the routine physical examination, but students should learn how to handle each joint properly and a formal examination is an important part of the evaluation of patients who present with joint symptoms or who have an established diagnosis and active symptoms. Diseases of the extra-articular soft tissues are particularly common.

Principles of joint examination

Certain general rules apply to the examination of all the joints and they can be summarised as: look, feel, move, measure, and compare with the opposite side.

Look

The first principle is always to compare right with left. Remember that joints are three-dimensional structures and need to be inspected from the front, the back and the sides. The skin is inspected for erythema indicating underlying inflammation and suggesting active, intense arthritis or infection, atrophy suggesting chronic underlying disease, scars indicating previous operations such as tendon repairs or joint replacements, and rashes. For example, psoriasis is associated with a rash and polyarthritis (inflammation of more than one joint). The psoriatic rash consists of scaling erythematous plaques on extensor surfaces. The nails are often also affected (page 252). Also look for a vasculitic skin rash (inflammation of the blood vessels of the skin), which can range in appearance from palpable purpura or livedo reticularis (bluish-purple streaks in a net-like pattern) to skin necrosis.

A small, firm, painless swelling over the back (dorsal surface) of the wrist is usually a synovial cyst—a ganglion.c A larger, localised, soft area of swelling of the dorsum of the wrist generally indicates tenosynovitis.

Note any swelling over the joint. There are a number of possible causes: these include effusion into the joint space, hypertrophy and inflammation of the synovium (e.g. rheumatoid arthritis), or bony overgrowths at the joint margins (e.g. osteoarthritis). It may also occur when tissues around the joints become involved, as with the tendinitis or bursitis of rheumatoid arthritis. Swelling of the lower legs may be due to fluid retention, which is painless and can occur in association with inflammation anywhere in the leg. Painful swelling may result from inflammation of the ankle joints or tendons, or of the fascia, or from inflammatory oedema of the skin and subcutaneous tissue.

Deformity is the sign of a chronic, usually destructive, arthritis, and ranges from mild ulnar deviation of the metacarpophalangeal joints in early rheumatoid arthritis to the gross destruction and disorganisation of a denervated (Charcot’sd) joint (Figure 10.20, page 319). Deviation of the part of the body away from the midline is called valgus deformity, and towards the midline, varus deformity. For example, genu valgum means knock-kneed and genu varum, bow-legged.

Look for abnormal bone alignment. Subluxation is said to be present when displaced parts of the joint surfaces remain partly in contact. Dislocation is used to describe displacement where there is loss of contact between the joint surfaces.

Muscle wasting results from a combination of disuse of the joint, inflammation of the surrounding tissues and sometimes nerve entrapment. It tends to affect muscle groups adjacent to the diseased joint (e.g. quadriceps wasting with active arthritis of the knee) and is a sign of chronicity.

Feel

Palpate for skin warmth. This is done traditionally with the backs of the fingers where temperature appreciation is said to be better. A cool joint is unlikely to be involved in an acute inflammatory process. A swollen and warm joint may be affected by active synovitis (see below), infection (e.g. Staphylococcus) or crystal arthritis (e.g. gout).

Tenderness is a guide to the acuteness of the inflammation, but may be present over the muscles of patients with fibromyalgia. The patient must be told to let the examiner know if the examination is becoming uncomfortable. Tenderness can be graded as follows:

This may result from joint inflammation or from lesions outside the joints (periarticular tissues), including inflamed tendons, bursae, or attachments (entheses). Infected joints are extremely tender and patients will often not let the examiner move the joint at all. Palpation of a joint or area for tenderness must be performed gently, and the patient’s face rather than the joint itself should be watched for signs that the examination is uncomfortable.

Palpate the joint deliberately now, if possible, for evidence of synovitis, which is a soft and spongy (boggy) swelling. This must be distinguished from an effusion, which tends to affect large joints but can occur in any joint. Here the swelling is fluctuant and can be made to shift within the joint. Bony swelling feels hard and immobile, and suggests osteophyte formation or subchondral bone thickening.

Assessment of individual joints

The hands and wrists (Figures 9.5 to 9.9)

Examination anatomy

The articulations between the phalanges are synovial hinge joints. The eight bones of the wrist (carpal bones) form gliding joints which allow wrist movements—flexion/extension and abduction/adduction as they slide over each other.

image

Figure 9.6 (right) X-ray of normal hand

Courtesy M Thomson, National Capital Diagnostic Imaging, Canberra.

Look

Start the examination at the wrists and forearms. Inspect the skin for erythema, atrophy, scars and rashes. Look for swelling and its distribution. Next look at the wrist for swelling, deformity, ulnar and hyloid prominence. Then look for muscle wasting of the intrinsic muscles of the hand. This results in the appearance of hollow ridges between the metacarpal bones. It is especially obvious on the dorsum of the hand.

Go on to the metacarpophalangeal joints. Again note any skin abnormalities, swelling or deformity. Look especially for ulnar deviation and volar (palmar) subluxation of the fingers. Ulnar deviation is deviation of the phalanges at the metacarpophalangeal joints towards the medial (ulnar) side of the hand. It is usually associated with anterior (Volar) subluxation of the fingers (Figure 9.10). These deformities are characteristic but not pathognomonic of rheumatoid arthritis (Table 9.9).

TABLE 9.9 Differential diagnosis of a deforming polyarthropathy

Rheumatoid arthritis
Seronegative spondyloarthropathy, particularly psoriatic arthritis, ankylosing spondylitis or Reiter’s disease
Chronic tophaceous gout (rarely symmetrical)
Primary generalised osteoarthritis
Erosive or inflammatory osteoarthritis

Next inspect the proximal interphalangeal and distal interphalangeal joints. Again note any skin changes and joint swelling. Look for the characteristic deformities of rheumatoid arthritis. These include swan neck and boutonnière deformity of the fingers and Z deformity of the thumb (Figure 9.10). They are due to joint destruction and tendon dysfunction. The swan neck deformity is hyperextension at the proximal interphalangeal joint and fixed flexion deformity at the distal interphalangeal joint. It is due to subluxation at the proximal interphalangeal joint and tendon shortening at the distal interphalangeal joint. The boutonnière (buttonhole) deformity consists of fixed flexion of the proximal interphalangeal joint and extension of the distal interphalangeal joints. This is due to protrusion of the proximal interphalangeal joint through its ruptured extensor tendon. The Z deformity of the thumb consists of hyperextension of the interphalangeal joint and fixed flexion and subluxation of the metacarpophalangeal joint.

Now look for the characteristic changes of osteoarthritis (Figure 9.11). Here the distal interphalangeal and first carpometacarpal joints are usually involved. Heberden’s nodese are a common deformity caused by marginal osteophytes that lie at the base of the distal phalanx. Less commonly, the proximal interphalangeal joints may be involved and osteophytes here are called Bouchard’sf nodes.

Look also to see if the phalanges appear sausage-shaped. This is characteristic of psoriatic arthropathy, but can also occur in patients with Reiter’s disease. It is due to interphalangeal arthritis and flexor tendon sheath oedema. Finger shortening due to severe destructive arthritis also occurs in psoriatic disease and is called arthritis mutilans. The hand may take up a main en lorgnette (‘hand holding long-handled opera glasses’) appearance due to a combination of shortening and telescoping of the digits.

Now examine the nails. Characteristic psoriatic nail changes may be visible: these include pitting (small depressions in the nail), onycholysis (Figure 9.12) and, less commonly, hyperkeratosis (thickening of the nail), ridging and discoloration. The presence of vasculitic changes around the nailfolds implies active disease. These consist of black to brown 1–2 mm lesions due to skin infarction and occur typically in rheumatoid arthritis (Figure 9.13). Splinter haemorrhages may be present in patients with systemic lupus erythematosus (and infective endocarditis) and are due to vasculitis. Unlike nailfold infarcts they are located under the nails in the nail beds. Periungual telangiectasiae occur in systemic lupus erythematosus, scleroderma or dermatomyositis.

The hands should now be turned over and the palmar surfaces revealed. Look at the palms for scars (from tendon repairs or transfers), palmar erythema, and muscle wasting of the thenar or hypothenar eminences (due to disuse, vasculitis or peripheral nerve entrapment). Telangiectasia here would support the diagnosis of scleroderma.

Feel and move

Turn the hands back again to the palm-down position. Palpate the wrists with both thumbs placed on the dorsal surface by the wrists, supported underneath by the index fingers (Figure 9.14). Feel gently for synovitis (boggy swelling) and effusions. The wrist should be gently dorsiflexed (normally possible to 75 degrees) and palmar flexed (also possible to 75 degrees) with the examiner’s thumbs. Then radial and ulnar deviation (20 degrees) is tested (Figure 9.15). Note any tenderness or limitation of movement or joint crepitus. Palpate the ulnar styloid for tenderness, which can occur in rheumatoid arthritis.

Test for tenderness at the tip of the radial styloid. This suggests de Quervain’sg tenosynovitis.

Feel for tenderness in the anatomical snuff box if scaphoid injury is suspected (Figure 9.15). Test for tenderness distal to the head of the ulna for extensor carpi ulnaris tendinitis.

Go on now to the metacarpophalangeal joints, which are palpated in a similar way with the two thumbs. Again passive movement is tested. Volar subluxation can be demonstrated by flexing the metacarpophalangeal joint with the proximal phalanx held between the thumb and forefinger. The metacarpophalangeal joint is then rocked backwards and forwards (Figure 9.16). Very little movement occurs with this manoeuvre at a normal joint. Considerable movement may be present when ligamentous laxity or subluxation is present.

Palpate the proximal and distal interphalangeal joints for tenderness, swelling and osteophytes.

Next test for palmar tendon crepitus. The palmar aspects of the examiner’s fingers are placed against the palm of the patient’s hand while he or she flexes and extends the metacarpophalangeal joints. Inflamed palmar tendons can be felt creaking in their thickened sheaths and nodules can be palpated. This indicates tenosynovitis.

A trigger finger may also be detected by this manoeuvre. Here the thickening of a section of digital flexor tendon is such that it tends to jam when passing through a narrowed part of its tendon sheath. Rheumatoid arthritis is an important cause. Typically, flexion of the finger occurs freely up to a certain point where it sticks and cannot be extended (as flexors are more powerful than extensors). The application of greater force overcomes the resistance with a snap.

If the carpal tunnel syndrome is suspected, ask the patient to flex both wrists for 30 seconds—paraesthesiae will often be precipitated in the affected hand if the syndrome is present (Phalen’sh wrist flexion test). The paraesthesiae (pins and needles) are in the distribution of the median nerve (page 363), when thickening of the flexor retinaculum has entrapped the nerve in the carpal tunnel (Table 9.10). This test is more reliable than Tinel’s sign,i in which tapping over the flexor retinaculum (which lies at the proximal part of the palm) may cause similar paraesthesiae.4

TABLE 9.10 Causes of carpal tunnel syndrome

Now test active movements. First assess wrist flexion and extension as shown in Figure 9.17. Compare the two sides. Now go on to thumb movements (Figure 9.18). The patient holds the hand flat, palm upwards, and the examiner’s hand holds the patient’s fingers. Test extension by asking the patient to stretch the thumb outwards, abduction by asking for the thumb to be pointed straight upwards, adduction by asking him or her to squeeze the examiner’s finger, and opposition by getting the patient to touch the little finger with the thumb. Look for limitation of these movements and discomfort caused by them. Next test metacarpophalangeal and interphalangeal movements. As a screening test, ask the patient to make a fist then to straighten out the fingers (Figure 9.19). Then test the fingers individually. If active flexion of one or more fingers is reduced, test the superficial and profundus flexor tendons (Figure 9.20). Hold the proximal finger joint extended and instruct the patient to bend it; the distal fingertip will flex if the flexor profundus is intact. Then hold the other fingers extended (to inactivate the profundus) and check finger flexion (inability indicates the superficialis is unable to work). The most common tendon ruptures are of the extensors of the fourth and fifth fingers.

Function

It is important to test the function of the hand. Grip strength is tested by getting the patient to squeeze two of the examiner’s fingers. Even an angry patient will rarely cause pain if given only two fingers. Serial measurements of grip strength can be made by asking the patient to squeeze a partly inflated sphygmomanometer cuff and noting the pressure reached. Key grip (Figure 9.21) is the grip with which a key is held between the pulps of the thumb and forefinger. Ask the patient to hold this grip tightly and try to open up his or her fingers. Opposition strength (Figure 9.22) is where the patient opposes the thumb and individual fingers. The difficulty with which these can be forced apart is assessed. Finally, a practical test, such as asking the patient to undo a button or write with a pen, should be performed.

Tests of hand function should be completed by formally assessing for neurological changes (page 362).

Examination of the hands is not complete without feeling for the subcutaneous nodules of rheumatoid arthritis near the elbows (Figure 9.23). These are 0.5–3 cm firm, shotty, non-tender lumps which occur typically over the olecranon. They may be attached to bone. They are found in rheumatoid-factor-positive rheumatoid arthritis. Rheumatoid nodules are areas of fibrinoid necrosis with a characteristic histological appearance and are probably initiated by a small vessel vasculitis. They are localised by trauma but can occur elsewhere, especially attached to tendons, over pressure areas in the hands or feet, in the lung, pleura, myocardium or vocal cords. The combination of arthritis and nodules suggests the diagnostic possibilities listed in Table 9.11.

TABLE 9.11 Causes of arthritis plus nodules*

Rheumatoid arthritis
Systemic lupus erythematosus (rare)
Rheumatic fever (Jaccoud’s arthritis) (very rare)
Granulomas—e.g. sarcoidosis (very rare)

* Gouty tophi and xanthomata from hyperlipidaemia may cause confusion.

François Jaccoud (1830–1913), professor of medicine, Geneva.

The elbows

Examination

Watch as the patient undresses, for difficulty disentangling the arms from clothing. The upper arms should be exposed completely. Note any deformity or difference in the normal 5–10 degree valgus position (carrying angle) as the patient stands with the palms facing forward.

Look for a joint effusion, which appears as a swelling on either side of the olecranon. Discrete swellings over the olecranon or over the proximal subcutaneous border of the ulna may be due to rheumatoid nodules, gouty tophi, an enlarged olecranon bursa or, rarely, to other types of nodules (Table 9.11).

Feel for tenderness, particularly over the lateral and medial epicondyles which may indicate tennis or golfer’s elbow, respectively. Palpate any discrete swellings. Rheumatoid nodules are quite hard, may be tender and are attached to underlying structures. Gouty tophi have a firm feeling and often appear yellow under the skin, but are sometimes difficult to distinguish from rheumatoid nodules. A fluid collection in the olecranon bursa is softly fluctuant and may be tender if inflammation is present. These collections are associated with rheumatoid arthritis and gout, but often occur independently of these diseases.

Small amounts of fluid or synovitis of the elbow joint may be detected by the examiner, facing the patient, placing the thumb of the opposite hand along the edge of the ulnar shaft just distal to the olecranon where the synovium is closest to the surface. Full extension of the elbow joint will cause a palpable bulge in this area if fluid is present.

Move the elbow joints passively. The elbow is a hinge joint. The zero position is when the arm is fully extended (0 degrees). Normal flexion is possible to 150 degrees. Limitation of extension is an early sign of synovitis.

If lateral epicondylitis is suspected, ask the patient to extend the wrist actively against resistance (see Figure 9.70, page 291). Test the range of active movements by standing in front of the patient and demonstrating. If there is any deformity or complaint of numbness, a neurological examination of the hand and arm are indicated for ulnar nerve entrapment.

History

Pain is the most common symptom of a patient with shoulder problems.5 Typically it is felt over the front and lateral part of the joint. It may radiate to the insertion of the deltoid or even further. Pain felt over the top of the shoulder is more likely to come from the acromioclavicular joint or from the neck. Deformity has to be severe before it becomes obvious. Pain and stiffness may severely limit shoulder movement. Instability may cause the alarming feeling that the shoulder is jumping out of its socket. This is most likely to occur during abduction and external rotation (e.g. while attempting to serve a tennis ball). Loss of function may result in difficulty using the arms at above shoulder height or reaching around to the back.

Examination

Watch the patient undressing and note forward, backward and upward movements of the shoulders and whether these seem limited or cause the patient pain. Stand back and compare the two sides. The arms should be held at the same level and the outlines of the acromioclavicular joints should be the same. There may be wasting of one of the deltoid muscles that will not be obvious unless the two are compared.

Look at the joint. A swelling may be visible anteriorly, but unless effusions are large and the patient is thin these are difficult to detect. Look for asymmetry and for scars as a result of injury or previous surgery.

Feel for tenderness and swelling. Stand beside the patient, rest one hand on the shoulder and move the arm into different positions (see below). As the shoulder moves, feel the acromioclavicular joint and then move the hand along the clavicle to the sternoclavicular joint.

Move the joint (Figures 9.26 and 9.27). The zero position is with the arm hanging by the side of the body so that the palm faces forwards. Abduction tests glenohumeral abduction, which is normally possible to 90 degrees. For the right shoulder the examiner stands behind the patient resting the left hand on the patient’s shoulder, while the right hand abducts the elbow from the shoulder. Elevation is usually possible to 180 degrees when it is performed actively, as movement of the scapula is then included. Adduction is possible to 50 degrees. The arm is carried forwards across the front of the chest. External rotation is possible to 65 degrees. With the elbow bent to 90 degrees the arm is turned laterally as far as possible. Internal rotation is usually possible to 90 degrees. It is tested actively by asking the patient to place his or her hand behind the back and then to try to scratch the back as high up as possible with the thumb. Patients with rotator cuff problems complain of pain when they perform this manoeuvre. Flexion is possible to 180 degrees, of which the glenohumeral joint contributes about 90 degrees. Extension is possible to 65 degrees. The arm is swung backwards as in marching. During all these manoeuvres, limitation with or without pain and joint crepitus are assessed.

Rapid assessment of shoulder movement is possible using the three-step ‘Apleyj scratch test’ (Figure 9.28). Stand behind and ask the patient to scratch an imaginary itch over the opposite scapula, first by reaching over the opposite shoulder, next by reaching behind the neck and finally by reaching behind the back.

The anterior stability of the shoulder joint is best assessed by the ‘apprehension’ test. Stand behind the patient, abduct, extend and externally rotate the shoulder (Figure 9.27c) while pushing the head of the humerus forwards with the thumb. The patient will strongly resist this manoeuvre if there is impending dislocation. There will be a similar response if the arm is adducted and internally rotated and posterior dislocation is about to occur.

This is also the time to test biceps function. The patient flexes the elbow against resistance. A ruptured biceps tendon causes the biceps muscle to roll up into a ball.

As a general rule, intra-articular disease produces painful limitation of movement in all directions, while tendinitis produces painful limitation of movement in one plane only, and tendon rupture or neurological lesions produce painless weakness. For example, if the abnormal sign is limited shoulder abduction in the middle range (45–135 degrees), this suggests ‘rotator cuff’ problems (i.e. the supraspinatus, infraspinatus, subscapularis and teres minor muscles) rather than arthritis.

In bicipital tendinitis there is localised tenderness on palpating over the groove. The supraspinatus tendon is a little higher, just under the anterior surface of the acromion. Supraspinatus tendinitis is common. Testing for it involves placing a finger over the head of the tendon while the shoulder is in extension. As this pushes the tendon forwards against the examiner’s finger, the movement is painful. When the shoulder is then flexed the tendon moves away and the pain disappears.

Don’t forget that arthritis affecting the acromioclavicular joint can be confused with glenohumeral disorders. Also remember to examine the neck and axillae in patients with shoulder pain.

The temporomandibular joints

Examination

Look in front of the ear for swelling. Feel by placing a finger just in front of the ear while the patient opens and shuts the mouth (Figure 9.29). The head of the mandible is palpable as it slides forwards when the jaw is opened. Clicking and grating may be felt. This is sometimes associated with tenderness if the joint is involved in an inflammatory arthritis. Rheumatoid arthritis may affect the temporomandibular joint.

The neck

Examination anatomy—the spine

The spinal column (Figure 9.30) is like a tower of bones that protects the spinal cord and houses its blood supply and efferent and afferent nerves. It provides mechanical support for the body and is flexible enough to allow bending and twisting movements. There are diarthrodial joints between the articular processes of the vertebral bodies, and the vertebral bodies are separated by the vertebral discs. These pads of cartilage are flexible enough to allow movement between the vertebrae. In the cervical spine from C3 to C7, the uncovertebral joints of Luschkak are present. These are formed between a lateral bony extension (uncinate process) from the margin of the more inferior vertebral body with the one above. Osteoarthritic hypertrophy of these joints may result in pain or nerve root irritation.

History

Pain is the most common neck symptom. Musculoskeletal neck pain usually arises in the structures at the back of the neck: the cervical spine, the splenius, semispinalis and trapezius muscles, or in the cervical nerves or nerve roots. Pain in the front of the neck may come from the oesophagus, trachea, thyroid gland or anterior neck muscles e.g. the sternocleidomastoid and platysma. Pain may be referred to the front of the neck from the heart.

There may be a history of trauma from direct injury or a sudden deceleration causing hyperextension of the neck; ‘whiplash’ injury. Injury can also be caused by attempted therapeutic neck manipulations by physiotherapists or chiropractors. The possibility of spinal cord injury must be considered in these patients. Ask about weakness or altered sensation in the arms and legs and any problem with bowel or bladder function.

The pain may have begun suddenly, suggesting a disc prolapse, or more gradually due to disc degeneration.

Postural tendon and muscle strains are common causes of temporary neck pain. These are often related to overuse. Ask for the patient’s occupation and whether work or recreational activities involve repeated and prolonged extension of the neck, e.g. painters and bicyclists. These patients often describe neck stiffness, and pain and muscle spasm are often present. The repeated holding of a telephone between the shoulder and the ear can cause nerve root problems. Neck movement may cause radicular symptoms such as paraesthesiae in the distribution of a cervical nerve after a hyperextension injury or cervical spine arthritis. Ask about paraesthesiae and weakness in the arms and hands.

Deformity may occur as a result of muscle spasm or sometimes following disc prolapse. Torticollis is a chronic and uncontrollable twisting of the neck to one side as a result of a muscle dystonia or cervical nerve root problem.

Examination

The patient should be undressed so as to expose the neck, shoulders and arms.

Look at the cervical spine while the patient is sitting up, and note particularly his or her posture (Figure 9.31). Movement should be tested actively. Flexion is tested by asking the patient to try to touch his or her chest with the chin (normal flexion is possible to 45 degrees). Extension (Figure 9.32a) is tested by asking the patient to look up and back (normally possible to 45 degrees). Lateral bending (Figure 9.32b) is tested by getting the patient to touch his or her shoulder with the ear; lateral bending is normally possible to 45 degrees. Rotation is tested by getting the patient to look over the shoulder to the right and then to the left. This is normally possible to 70 degrees.

Feel the posterior spinous processes. This is often easiest to do when the patient lies prone with the chest supported by a pillow and the neck slightly flexed. The examiner should feel for tenderness and uneven spacing of the spinous processes. Tenderness of the facet joints will be elicited by feeling a finger’s breadth lateral to the middle line on each side (Figure 9.33).

Neurological examination of the upper limbs, including testing of shoulder abduction (C5, C6) and the serratus anterior muscle (C5, C6, C7), is part of the assessment of the neck.

The thoracolumbar spine and sacroiliac joints

History

Lower back pain is a very common symptom (Table 9.12). The discomfort is usually worst in the lumbosacral area. Ask whether the onset was sudden and associated with lifting or straining or whether it was gradual.1,2 Stiffness and pain in the lower back that is worse in the morning is characteristic of an inflammatory spondyloarthropathy. Pain that shoots from the back into the buttock and thigh along the sciatic nerve distribution is called ‘sciatica. In sciatic nerve compression at a lumbosacral nerve root, the pain is often aggravated by coughing or straining. ‘Lumbago’ however is often due to referred pain (e.g. from the vertebral joints). There may be other neurological symptoms in the legs due to nerve compression or irritation. The distribution of the paraesthesiae or weakness may indicate the level of spinal cord or nerve root abnormality. One should also ask about urinary incontinence and retention as well as numbness in the ‘saddle region’, erectile dysfunction and bowel incontinence, which can be a result of cauda equina involvement.

TABLE 9.12 Differential diagnoses for back pain

Examination

To start the examination, have the patient standing and clothed only in underpants. Look for deformity, inspecting from both the back and side. Note especially loss of the normal thoracic kyphosis and lumbar lordosis, which is typical of ankylosing spondylitis. Also note any evidence of scoliosis, a lateral curvature of the spine which may be simple (‘C’ shaped) or compound (‘S’ shaped) and which can result from trauma, developmental abnormalities, vertebral body disease (e.g. rickets, tuberculosis) or muscle abnormality (e.g. polio).

Feel each vertebral body for tenderness and palpate for muscle spasm.1

Movement is assessed actively. Bending movements largely take place at the lumbar spine, while rotational movements occur at the thoracic spine. Range of movement is tested by observation (Figure 9.34) and the use of Schober’s test (see below) (Figure 9.35).

image

Figure 9.35 Schober’s test

From Douglas G, Nicol F and Robertson C, Macleod’s Clinical Examination, 12th edn. Edinburgh: Churchill Livingstone, 2009, with permission.

Flexion is tested by asking the patient to touch the toes with the knees straight. The normal range of flexion is very wide. Many people can reach only halfway down the shins when the knees are kept straight. As the patient bends, look at the spine: there is normally a gentle curve along the back from the shoulders to the pelvis. Patients with advanced ankylosing spondylitis have a flat ankylosed spine and all the bending occurs at the hips. Test extension by asking the patient to lean backwards. Patients with back pain usually find this less uncomfortable than bending forwards. Lateral bending is assessed by getting the patient to slide the right hand down the right leg as far as possible without bending forwards, and then the same for the left side. This movement tends to be restricted early in ankylosing spondylitis. Rotation is tested with the patient sitting on a stool (to fix the pelvis) and asking him or her to rotate the head and shoulders as far as possible to each side. This is best viewed from above.

Measure the lumbar flexion with Schober’s test (Figure 9.35). A mark is made at the level of the posterior iliac spine on the vertebral column (approximately at L5). One finger is placed 5 cm below and another 10 cm above this mark. The patient is then asked to touch the toes. An increase of less than 5 cm in the distance between the two fingers indicates limitation of lumbar flexion. The finger-to-floor distance at full flexion can be measured serially to give an objective indication of disease progression.

Assess straight leg raising (Lasègue’sl test includes passive ankle dorsiflexion). With the patient lying down, lift the straightened leg if sciatica is suspected (normally to 80–90 degrees). This will be limited by pain in lumbar disc prolapse (less than 60 degrees).

Press directly on the anterior superior iliac spines and apply lateral pressure so as to attempt to separate them. This will cause pain in the sacroiliac joints when patients have sacroiliitis.

Now get the patient to lie in bed on the stomach. Look for gluteal wasting. The sacroiliac joints lie deep to the dimples of Venus.m By tradition, firm palpation with both palms overlying each other is used to elicit tenderness in patients with sacroiliitis. Test each side separately.

Now ask the patient to lie on one side. Apply firm pressure to the upper pelvic rim. This will also elicit pain in the sacroiliac joints.

The complete examination of the back also requires neurological assessment of the lower limbs.6

The hips

A limp may be noticed by the patient. When associated with pain it is a compensating mechanism but, when painless, may be due to differing limb length or instability of the joint. Patients are sometimes aware of clicking or snapping coming from the region of the hip. This may be due to a psoas bursitis or to slipping of the tendon of the gluteus maximus over the edge of the greater trochanter. Functional impairment usually results in difficulty walking and climbing stairs. Sitting down and standing up can become progressively more uncomfortable because of stiffness and pain.

A history of a fall and inability to walk or bear weight on the leg suggests a fracture of the neck of the femur. A history of rheumatoid arthritis and pain which is present at rest suggests rheumatoid arthritis of the hip. Osteoarthritis is more likely to evolve gradually in older people and is associated with obesity and with recurrent trauma.

Ask about systemic symptoms such as fever and weight loss which might be a sign of septic arthritis.

Pain which is associated with paraesthesiae and radiates in the distribution of the lateral cutaneous nerve of the thigh suggests an entrapment syndrome (meralgia paraesthetica).

Examination

Watch the patient walking into the room and note the use of a walking stick, a slow and obviously uncomfortable gait, or a limp.

Get the patient to lie down, first on the back.

Looking at the hip joint itself is not possible because so much muscle overlies it. However, the examiner must inspect for scars and deformity. The patient may adopt a position with one leg rotated because of pain.

Feel just distal to the midpoint of the inguinal ligament for joint tenderness. This point lies over the only part of the femoral head that is not intra-acetabular. Now feel for the positions of the greater trochanters. The examiner’s thumbs are placed on the anterior superior iliac spines on each side while the fore and middle fingers move posteriorly to find the tips of the greater trochanters. These should be at the same level. If one side is higher than the other, the higher side is likely to be the abnormal one.

Move the hip joint passively (Figure 9.37). Flexion is tested by flexing the patient’s knee and moving the thigh towards the chest. The examiner keeps the pelvis on the bed by holding the other leg down. A fixed flexion deformity (inability to extend a joint normally) may be masked by the patient’s arching the back and tilting the pelvis forward and increasing lumbar lordosis unless Thomas’s testn is applied. The legs are fully flexed to straighten the pelvis. One leg is then extended. A fixed flexion deformity (e.g. as result of osteoarthritis) will prevent straightening. Rotation is tested with the knee and hip flexed. One hand holds the knee, the other the foot. The foot is then moved medially (external rotation of the hip, normally possible to 45 degrees), then laterally (internal rotation of the hip, normal to 45 degrees). Abduction is tested by standing on the same side of the bed as the leg to be tested. The right hand grasps the heel of the right leg while the left hand is placed over the anterior superior iliac spine to steady the pelvis. The leg is then moved outwards as far as possible. This is normally possible to 50 degrees. Adduction is the opposite. The leg is carried immediately in front of the other limb and this is normally possible to 45 degrees.

Ask the patient to roll over onto the stomach. Extension is then tested by placing one hand over the sacroiliac joint while the other elevates each leg. This is normally possible to about 30 degrees. Ask the patient to stand now and perform the Trendelenburgo test. The patient stands first on one leg and then on the other. Normally the non-weightbearing hip rises, but with proximal myopathy or hip joint disease the non-weightbearing side sags.

Finally, the true leg length (from the anterior superior iliac spine to the medial malleolus) and apparent leg length (from the umbilicus to the same lower point) for each leg should be measured. A difference in true leg length indicates hip disease on the shorter side, while apparent leg length differences are due to tilting of the pelvis.

In patients with osteoarthritis of the joint, internal rotation, abduction and extension are usually restricted.7 Osteoarthritic joints (Figure 9.38) show loss of joint space, sclerosis (thickening and increased radiodensity) at the joint margins and osteophyte (bony outgrowth) formation on plain X-ray films.

The knees

History (Table 9.14)

Pain is a common knee problem. If there has been an injury or it is due to a mechanical abnormality, it is often localised. Inflammatory diseases more often cause diffuse pain. Ask the patient to point to the place where the pain is most severe. Stiffness is usually of gradual onset and is typical of osteoarthritis. It tends to be worse after inactivity. Locking of the knee usually means there is a sudden inability to reach full extension. The knee is often stuck at about 45 degrees of flexion. Unlocking may occur just as suddenly, sometimes following some form of manipulation by the patient. The cause is mechanical: a loose body or torn meniscus has become wedged between the articular surfaces of the joint. Swelling may occur suddenly after an injury, suggesting it is due to haemarthrosis from a fracture or ligamentous tear; if swelling occurs after a few hours a torn meniscus is more likely to be the cause. Arthritis and synovitis cause a chronic swelling. Patients sometimes notice deformity, which in later life is usually due to arthritis. Sometimes the patient may complain that the knee is unstable or gives way. Patellar instability and ruptured ligaments may present this way. One should always ask about loss of function. There is often a reduced ability to walk distances, climb stairs and get into and out of chairs.

TABLE 9.14 Differential diagnosis of knee pain

Area of pain Associated features
Lateral aspect of knee
Tear of lateral meniscus History of trauma
Locking or clicking
Swelling delayed after injury
Tear of lateral collateral ligament Knee gives way
Biceps femoris strain Overuse or injury
Medial aspect of knee
Tear of medial meniscus History of trauma
Locking or clicking
Swelling delayed after injury
Tear or strain of medial collateral ligament Knee gives way
Hamstring strain Overuse or injury
Patellofemoral syndrome Overuse
Chronic symptoms
Back of the knee
Baker’s cyst Sudden pain
Localised swelling and tenderness
Bursitis, e.g. popliteal, semimembranosus Overuse pattern
Chronic pain
Hamstring strain Injury or overuse
Deep venous thrombosis  
Front of the knee
Patellar fracture Injury
Sudden pain and tenderness
Swelling
Separation of fractured segments, visible or palpable
Patellar tendinitis Overuse
Osteoarthritis Chronic pain
Worse with walking
History of old injuries
Prepatellar bursitis (housemaid’s knee*) Occupation
Infrapatellar bursitis (clergyman’s knee) Occupation

* Described by Henry Hamilton Bailey (1894–1961) as ‘the most elementary diagnosis in surgery’.

Osteoarthritis of the knee is very common. Older age, previous injury and stiffness lasting less than half an hour are in favour of this diagnosis as the cause of knee pain. Good signs guide 9.1 outlines the symptoms and signs of this condition. Physically active adolescents may present with pain and swelling below the knee at the point of attachment of the patellar tendon to the tibial tuberosity—tibial apophysitis or Osgood Schlatter’s disease.p This is the most common traction apophysitis.

GOOD SIGNS GUIDE 9.1 Osteoarthritis as the cause of chronic knee pain

Symptom or sign LR positive LR negative
Stiffness < 30 mins 3.0 0.2
Crepitus on passive movement 2.1 0.2
Bony enlargement 11.8 0.5
Palpable increase in temperature 0.3 1.6
Valgus deformity 1.4 0.9
Varus deformity 3.4 0.8
At least 3 of the above 3.1 0.1

From McGee S, Evidence-based physical diagnosis, 2nd edn. St Louis: Saunders, 2007.

Ask if there has been previous knee surgery or arthroscopy.

Take an occupational and sporting history. Injury and overuse syndromes are often related to exercise (particularly competitive sport) and occupations associated with repetitive minor injuries to the knees.

Examination

This is performed with the patient in a number of positions and, of course, walking.8,9 Even more than with the other joints, it is important to examine the more normal or uninjured knee first. This will help with the interpretation of changes in the other knee and give the patient more confidence that the examination will not be painful.

Look first with the patient lying down on the back with both knees and thighs fully exposed. The affected knee will often be flexed, the most comfortable position. Note any quadriceps wasting. This begins quite soon after knee abnormalities lead to disuse of the muscle. Examine the knees themselves for skin changes, scars (including those from previous surgery or arthroscopy), swelling and deformity. Compare each side with the other. Localised swellings may move about as the knee flexes and extends. They are often cartilaginous loose bodies. Fixed lumps in the line of the joint may be meniscal cysts.

Swelling of the synovium or a knee effusion is usually seen medial to the patella and in the joint’s suprapatellar extension. Loss of the peripatellar grooves may be an early sign of an effusion. Assess fixed flexion deformity by squatting down and looking at each knee from the side. A space under the knee will be visible if there is permanent flexion deformity arthritis.

Varus and valgus deformity may be obvious here but are more easily seen when the patient stands. Varus deformity is often related to osteoarthritis and valgus deformity to rheumatoid arthritis.

Now watch as the patient flexes and straightens each knee in turn. As the knee extends the patella glides upwards and remains centred over the femoral condyles. If there is patellar subluxation it will slip laterally during knee flexion and return to the midline during knee extension.

Feel the quadriceps for wasting. Palpate over the knees for warmth and synovial swelling.

Test carefully for a joint effusion. The patellar tap is used to confirm the presence of large effusions (Figure 9.40). One hand rests over the lower part of the quadriceps muscle and compresses the suprapatellar extension of the joint space. The other hand pushes the patella downwards. The sign is positive if the patella is felt to sink and then comes to rest with a tap as it touches the underlying femur. The bulge sign is used to detect small effusions. Here the left hand compresses the suprapatellar pouch while the fingers of the right hand are run along the groove beside the patella on one side and then the other. A bulging along the groove due to a fluid wave, on the side not being compressed, is a sign of a small effusion.

Examine for patellofemoral lesions by sliding the patella sideways across the underlying femoral condyles.

Move the joint passively. Test flexion (normally possible to 135 degrees) and extension (normal to 5 degrees) by resting one hand on the knee cap while the other moves the leg up and down (Figure 9.41a). The range of movements and the presence of crepitus are noted. While holding the knee flexed, feel for and attempt to localise tenderness. Feel gently for tenderness along the joint line at the patellar ligament and at the sites of attachment of the collateral ligaments.

Test the ligaments next. The lateral and medial collateral ligaments are assessed by having the knee slightly flexed while holding the leg, with the examiner’s forearm resting along the length of the tibia; lateral and medial movements of the leg on the knee joint are tested (Figure 9.41b). Meanwhile the thigh is steadied with the other hand. Movements of more than 5–10 degrees are abnormal. The cruciate ligaments (Figure 9.41c) are tested next. The examiner steadies the patient’s foot with an elbow or by sitting on it. The patient’s knee is flexed to 90 degrees. The examiner’s hands grasp the tibia and attempt anterior and posterior movements of the leg on the knee joint. Movement may be detected by the examiner’s thumbs positioned at the joint margins. Again, movement of more than 5–10 degrees is abnormal. Increased anterior movement suggests anterior cruciate ligamentous laxity, and increased posterior movement suggests posterior cruciate ligamentous laxity. The Lachman test may be more accurate (positive LR 42.0, negative LR 0.1).8 Here the knee is flexed 20–30 degrees while the patient is lying supine. Grasp the femur (place your hand above the knee) to steady it, then grab the lower leg below the knee and give it a quick forward tug. It is abnormal when there is exaggerated anterior tibial movement or the knee fails to stop with a thud.

When recurrent dislocation or subluxation of the patella is suspected, the patellar apprehension test should be performed. Push the patella firmly in a lateral direction while slowly flexing the knee. The patient’s face should be studied for the anxious look that suggests impending dislocation (it is then time to suspend the test).

Ask the patient to roll into the prone position. Look and feel in the popliteal fossa for a Baker’s cyst.q This is a pressure diverticulum of the synovial membrane that occurs through a hiatus in the knee capsule (Figure 9.42). It is best seen with the knee extended. Rupture of this into the calf muscle produces signs that may mimic a deep venous thrombosis. Rupture is often associated with the ‘crescent sign’— ecchymoses below the malleoli of the ankle. A Baker’s cyst must be distinguished from an aneurysm of the popliteal artery, which will be pulsatile, and a bony tumour (very hard).

This is also the position in which Apley’s grinding test may be performed (Figure 9.43). This is a test of meniscal damage. The patient’s leg is flexed to 90 degrees, the examiner stabilises the thigh by kneeling lightly on it and while pressing on the foot rotates the leg backwards and forwards. Pain or clicking make the test positive. The distraction test is the opposite. Here the patient’s leg is pulled upwards so as to take the strain off the menisci and stretch the ligaments. If the patient finds the test painful, a ligamentous abnormality may be the cause.

McMurray’sr test (Figure 9.44) is another way of detecting a meniscal tear. The patient lies on the back, the examiner stands on the side to be tested and holds the ankle. The examiner’s other hand sits on the medial side of the knee and pushes to apply valgus force. The patient’s leg is then extended from the flexed position while being internally and then externally rotated. The test is positive if there is a popping sensation, which may be followed by inability to extend the knee.

Stand the patient up. Look particularly for varus (bow-leg) and valgus (knock-knee) deformity.

Finish with a test of function. Get the patient to walk to and fro. Study the gait and the movement of the knees, particularly for a sideways wobble.

The ankles and feet

Patients with foot (Table 9.16) or ankle pain may have a history of rheumatoid arthritis. This can cause pain and deformity and affect the ankle subtalar, midtarsal and metatarsophalangeal joints.

TABLE 9.16 Differential diagnoses of foot pain

Very severe pain involving the first metatarsophalangeal joint is usually due to gout. Pain right over one of the metatarsals that comes on after unusually vigorous exercise may be due to a stress fracture.

There may be deformity involving the ankle or toes. Patients find this especially troublesome if it makes it difficult to put on shoes. The patient may have noticed swelling; ask if this is painful or not and whether it involves one or both feet. Bilateral swelling is more likely due to inflammation. Swelling over the medial aspect of the first metatarsal head (a bunion) occurs commonly as people get older, but may be associated with rheumatoid arthritis.

Paraesthesiae in the feet may have been noticed. Try to find out the distribution of the abnormal sensation, which may be a result of peripheral nerve injury or peripheral neuropathy. Coldness of the feet is very common but cyanosis and ulceration are more worrying problems. Chronic foot ulcers mean diabetes must be excluded.

Examination

This examination includes the ankles, feet and toes.

Look at the skin. Note any swelling, scars, deformity or muscle wasting. Deformities affecting the forefoot include hallux valgus (fixed lateral deviation of the main axis of the big toe), clawing (fixed flexion deformity) and crowding of the toes, as occurs in rheumatoid arthritis. Sausage deformities of the toes occur with psoriatic arthropathy or Reiter’ss disease (Figure 9.46). Look for the nail changes that suggest psoriasis. Inspect the transverse arch of the foot, which runs underneath the metatarsophalangeal joints, and the longitudinal arch, which runs from the first metatarsophalangeal joint to the heel. These arches, which bear the weight of the body, may be flattened in arthritic conditions of the foot like rheumatoid arthritis. Calluses over the metatarsal heads on the plantar surface of the foot occur with subluxation of these joints (Figure 9.47).

Feel, starting with the ankle, for swelling around the lateral and medial malleoli. This should not be confused with pitting oedema. If an ankle fracture is suspected because of a history of injury, tenderness over the posterior medial malleolus is a reliable sign (positive LR 4.8).10

Move the talar (ankle) joint, grasping the midfoot with one hand. Dorsiflexion is tested by raising the foot towards the knee—normally possible to 20 degrees—and plantar flexion by performing the opposite manoeuvre, which is normally possible to 50 degrees.

With the subtalar joint, only inversion and eversion of the foot on the ankle are tested. Pain on movement is more important than range at this joint. The midtarsal (midfoot) joint allows rotation of the forefoot when the hindfoot is fixed. This is done by steadying the ankle with one hand and rotating (twisting) the forefoot. Again, pain on motion rather than loss of range of movement is noted.

Squeeze the metatarsophalangeal joints by compressing the first and fifth metatarsals between your thumb and forefinger. Tenderness suggests inflammation, common in early rheumatoid arthritis. Press upwards from the sole of the foot just proximal to the metatarsophalangeal joints of the third and fourth toes. Pain here suggests Morton’st neuroma. This is due to entrapment and swelling of the digital nerve between the toes. It is associated with pain and numbness of the sides of these toes.

Each individual interphalangeal joint is then assessed by feeling and moving. These are typically affected in the seronegative spondyloarthropathies. Extremely tender involvement of the first metatarsophalangeal joint is characteristic of acute gout. In this case the joint also looks red and swollen.

Palpate the Achilles tendon for rheumatoid nodules (Figure 9.48) and tenderness due to Achilles tendinitis. An old Achilles tendon rupture may be detected by squeezing the calf: normally the foot plantar flexes unless the tendon has previously ruptured (Simmonds’u test). Also palpate the inferior aspect of the heel for tenderness; this may indicate plantar fasciitis, which occurs in the seronegative spondyloarthropathies and sometimes for no apparent reason.

Correlation of physical signs and rheumatological disease

Rheumatoid arthritis (Figures 9.30 and 9.49)

This is a chronic systemic inflammatory disease of unknown aetiology which characteristically involves the joints. In the majority of cases, patients with rheumatoid arthritis have rheumatoid factor present in the serum (seropositive disease). These are heterogeneous antibodies directed against the Fc portion of immunoglobulin G (IgG), but are not specific for rheumatoid arthritis.

To examine the patient with suspected rheumatoid arthritis, sit him or her up in bed or on a chair.

General inspection

Look to see whether the patient has a Cushingoid appearance due to steroid treatment (page 309), or whether there are signs of weight loss that may indicate active disease.

The chest

Now examine the lungs for signs of pleural effusions or pulmonary fibrosis. Caplan’s syndromev is the presence of rheumatoid lung nodules in combination with pneumoconiosis.

Seronegative spondyloarthropathies

Four conditions are generally accepted as belonging to this group: ankylosing spondylitis, psoriatic arthritis, Reiter’s disease (reactive arthritis) and enteropathic arthritis. These are called the seronegative spondyloarthropathies because they were originally distinguished from rheumatoid arthritis by the absence of rheumatoid factor in the serum. However, up to 30% of patients with otherwise classical rheumatoid arthritis are rheumatoid factor negative. The seronegative spondyloarthropathies overlap clinically and pathologically, and have an association with HLA-B27.

Ankylosing spondylitis

The following areas should be examined.

The back and sacroiliac joints: may show loss of lumbar lordosis and thoracic kyphosis; severe flexion deformity of the lumbar spine (rare); tenderness of the lumbar vertebrae; reduction of movement of the lumbar spine in all directions; and tenderness of the sacroiliac joints.

The legs: Achilles tendinitis; plantar fasciitis; signs of cauda equina compression (rare)—lower limb weakness, loss of sphincter control, saddle sensory loss.

The lungs: decreased chest expansion (less than 5 cm); signs of apical fibrosis.

The heart: signs of aortic regurgitation.

The eyes: acute iritis (tends to recur)—painful red eye (10%–15%) (Figure 9.51).

Rectal and stool examination: signs of inflammatory bowel disease (either ulcerative colitis or Crohn’s disease). Note: signs of secondary amyloidosis—for example, hepatosplenomegaly, renal enlargement, proteinuria—may be present, although this is a very rare complication.

X-rays of the spine and sacroiliac joints (Figure 9.52): may show ankylosis (fusion) of the sacroiliac joints and ‘squaring’ of the vertebral bodies as a result of loss of their anterior corners and periostitis of their waists. ‘Bridging syndesmophytes’w occur as a result of ossification of the fibres of the joint annulus. Severe disease causes the changes called bamboo spine visible on X-ray.

Reiter’s syndrome (reactive arthritis)

Classically this disease follows urethritis or diarrhoea, with conjunctivitis and arthritis (usually asymmetrical) of the large weightbearing joints such as the hip, knee or ankle. The following areas should be examined.

The genital region: urethral discharge; circinate balanitis—scaly, superficial reddened erosions with well-demarcated borders on the glans penis (Figure 9.53).

The prostate: prostatitis.

The eyes: conjunctivitis; iritis (rare).

The mouth: painless smooth mucosal lesions, especially of the tongue.

The back: sacroiliac joints (may be unilaterally involved).

The lower limbs (more commonly affected): knees, ankles; metatarsophalangeal joints and toes (‘sausage toes’); plantar fasciitis, Achilles tendinitis; keratoderma blennorrhagica on the sole (non-tender reddish-brown macules, which become scaling papules; Figure 9.54)—this is indistinguishable from pustular psoriasis; nails thickened, opaque and brittle.

image

Figure 9.54 Reiter’s syndrome with keratoderma blennorrhagica

From FS McDonald, ed., Mayo Clinic images in internal medicine, with permission. © Mayo Clinic Scientific Press and CRC Press.

The hands (less commonly involved): wrists; metacarpophalangeal joints, proximal interphalangeal joints, distal interphalangeal joints; keratoderma blennorrhagica on the palms; nail changes.

Cardiovascular system: aortic regurgitation (rare).

X-ray findings: the first attack of arthritis is associated with soft-tissue changes and subsequent attacks may lead to joint-space narrowing and proliferative erosions at the joint margins. Changes in the sacroiliac joints and spine resemble those of ankylosing spondylitis except that the sacroiliac joint changes and spinal syndesmophytes tend to be asymmetrical. Calcaneal spurs (Figure 9.55)—a result of plantar fasciitis—are characteristic.

Psoriatic arthritis

Ten per cent of patients with psoriasis (page 446) have arthritis.

Examine as for rheumatoid arthritis, but include the spine and sacroiliac joints. There are five distinct groups of psoriatic arthritis, but overlap is common.

X-ray findings (Figure 9.56): in mild cases X-rays are normal or show only joint-space narrowing and erosive changes. Unlike the X-rays of rheumatoid joints the bone density is maintained and there may be sclerotic changes in the small bones. Ankylosis of peripheral joints and arthritis mutilans can occur in either condition. The involvement of the spine and sacroiliac joints is asymmetrical, as in Reiter’s syndrome.

Gouty arthritis

Begin with the feet, as acute gouty arthritis affects the metatarsophalangeal joint of the great toe in 75% of cases. Next examine the ankles and knees, which tend to be involved after recurrent attacks. The fingers, wrists and elbows are affected late (Figure 9.57). Inspect and palpate for gouty tophi (these are urate deposits with inflammatory cells surrounding them) (Latin tophus, ‘chalk stone’). The presence of tophi indicates chronic recurrent gout. They tend to occur over the joint synovia, the olecranon bursa, the extensor surface of the forearm, the helix of the ear (Figure 9.58), and in the infrapatellar and Achilles tendons.

Finally, examine for signs of the causes of secondary gout: increased purine turnover due to myeloproliferative disease (page 236), lymphoma (page 237) or leukaemia; and decreased renal urate excretion due to renal disease or hypothyroidism. Hypertension, diabetes mellitus and ischaemic heart disease are more common among sufferers of gout.

X-rays (Figure 9.59) show multiple juxta-articular erosions which may obliterate the joint space.

Systemic lupus erythematosus (SLE)

This is a multisystemic chronic inflammatory disease of unknown origin, named because the erosive nature of the condition was likened to the damage caused by a hungry wolf (Latin lupusx ‘wolf’) (Figure 9.60).

Forearms

Livedo reticularis may occur here; in Latin this describes skin discoloration in the form of a small net. This is formed by connected bluish-purple streaks without discrete borders. They occur usually on the limbs and are associated with various connective tissue diseases.11 Look for purpura (due to vasculitis12 or autoimmune thrombocytopenia). Examine for a proximal myopathy (due to the disease itself or to steroid treatment). Subcutaneous nodules very rarely occur in SLE. The axillary nodes may be enlarged but will not be tender.

The head and neck

Alopecia (hair loss) is an important diagnostic clue that occurs in about two-thirds of patients and may be associated with scarring. Look especially for lupus hairs, which are short, broken hairs above the forehead. The hair as a whole may be coarse and dry, as in hypothyroidism.

Examine the eyes for scleritis and episcleritis (see Figure 9.50). The eyes may be red and dry (Sjögren’s syndrome). Pallor of the conjunctivae occurs with anaemia, usually due to chronic disease. Occasionally jaundice due to autoimmune haemolytic anaemia may be found. Perform a fundoscopy for cytoid bodies, which are hard exudates (white spots) due to aggregates of swollen nerve fibres and are secondary to vasculitis.

A facial rash may be diagnostic (Figure 9.61). The classical rash is an erythematous ‘butterfly rash’ over the cheeks and bridge of the nose and must be distinguished from rosacea. Mouth ulcers on the soft or hard palate may occur and the mouth may be dry (Sjögren’s syndrome).

The rash of discoid lupus may be found in the same area or affect different parts of the body. Lesions begin as spreading red plaques which have a central area of hyperkeratosis and follicular plugging. An active lesion has an oedematous edge. The appearance may suggest psoriasis. A healed lesion may have marginal hyperpigmentation with central atrophy and depigmentation. The scalp, external ear and face are most commonly affected, but in some patients lesions may occur all over the arms and chest. Extensive annular or psoriaform lesions may indicate the presence of subacute cutaneous lupus.

After examining the face, feel for cervical lymphadenopathy, which is usually non-tender.

The legs

Examine for proximal myopathy and peripheral neuropathy (mainly sensory).

Rarely there may be signs of hemiplegia, cerebellar ataxia or chorea.

Leg ulceration over the malleoli, due to vasculitis or the antiphospholipid syndrome,11 is important. Very occasionally the toes may be gangrenous. There may be ankle oedema from the nephrotic syndrome or fluid retention from steroids. Livedo reticularis may be present on the legs.

Scleroderma (progressive systemic sclerosis)

This is a disorder of connective tissue with variable cutaneous fibrosis and with abnormalities of the microvasculature of the fingers, gut, lungs, heart and kidneys. In diffuse cutaneous scleroderma there is more prominent skin sclerosis and these patients may have pulmonary fibrosis. In limited cutaneous scleroderma (CREST syndrome—Calcinosis, Raynaud’s phenomenon, o Esophageal motility disturbance, Sclerodactyly and Telangiectasia), diffuse skin sclerosis and interstitial lung disease do not occur but patients are at risk of developing pulmonary hypertension.

General inspection (Figure 9.62)

Look for cachexia due to dysphagia (from an oesophageal motility disturbance) or malabsorption (due to bacterial overgrowth).

Skin changes in scleroderma vary. There may be an early oedematous phase with non-tender pitting oedema of the hands which appear tightly swollen. In patients with progressive disease the oedematous skin is replaced by indurated skin which appears thickened, hard and tight. This phase usually begins in the fingers (Table 9.17).

TABLE 9.17 Differential diagnosis of thickened tethered skin

Systemic sclerosis (scleroderma), diffuse type; milder changes in limited cutaneous scleroderma
Mixed connective tissue disease (a distinct disorder with features of scleroderma, systemic lupus erythematosus, rheumatoid arthritis and myositis)
Eosinophilic fasciitis—widespread skin thickening due to inflammation of the fascia often following excessive muscle exercise; occurs in association with eosinophilia and hypergammaglobulinaemia
Localised morphea—heterogeneous group of disorders where there are small areas of sclerosis: most common type is morphea, which begins with large plaques of red or purple skin that evolve into sclerotic areas and may regress spontaneously over years
Chemically induced: vinyl chloride, pentazocine, bleomycin
Pseudoscleroderma: porphyria cutanea tarda, acromegaly, carcinoid syndrome
Scleroedema: thickened skin over the shoulders and upper back in diabetes mellitus
Graft versus host disease
Silicosis
Eosinophilic myalgia syndrome (L-tryptophan)
Toxic oil syndrome

The hands

Examine the hands. Note particularly calcinosis (palpable nodules due to calcific deposits in the subcutaneous tissue of the fingers), Raynaud’s phenomenon sometimes causing atrophy of the finger pulps (due to ischaemia) (Figure 9.63), sclerodactyly (tightening of the skin of the fingers leading to tapering), and multiple large telangiectasia on the fingers (Figure 9.64).

Look for contraction deformity of the fingers, which is relatively common (Figure 9.65), and for synovitis, although this is uncommon. The nails can be affected by Raynaud’s. It can be useful to inspect the nailfolds using a hand-held magnifying glass: in scleroderma you may see dilated capillary loops but this is not diagnostic. These are best viewed on the fourth digit. Assessing hand function is important in this disease.

Rheumatic fever

This is an inflammatory disease which is a delayed sequel to infection with group A beta-haemolytic Streptococcus; it is uncommon in Western nations today. It is diagnosed by finding two major or one major and two minor criteria, plus evidence of recent streptococcal infection.

Major criteria: (i) carditis (causing tachycardia, murmurs, cardiac failure, pericarditis); (ii) polyarthritis; (iii) chorea (page 399); (iv) erythema marginatum (see below); (v) subcutaneous nodules (painless mobile swellings).

Minor criteria: (i) fever; (ii) arthralgia; (iii) previous rheumatic fever; (iv) acute phase proteins; (v) prolonged PR interval on the ECG.

The vasculitides

This is a heterogeneous group of disorders characterised by inflammation and damage to blood vessels.12 The clinical features and major vessels involved are shown in Table 9.18.

TABLE 9.18 The vasculitides

Name Vessels Characteristics
Small vessel vasculitis
Wegener’s* granulomatosis Small to medium-sized capillaries, venules, arterioles, small arteries Granulomatous inflammation affecting the respiratory tract, often with necrotising glomerulonephritis
Saddle-nose deformity
Churg-Strauss syndrome Small Asthma, eosinophilia, skin nodules, mononeuritis multiplex, pulmonary infiltrates
Henoch-Schonlein purpura Small Children affected; purpura over buttocks, abdominal pain, arthritis of knee and ankle, nephritis (40%)
Microscopic polyangiitis Small Glomerulonephritis, alveolar haemorrhage, neuropathy, pleural effusions
Mixed essential cryoglobulinaemia Small Arthritis, palpable purpura of extremities, Raynaud’s disease, neuropathy
Hepatitis C common
Medium-sized vessel vasculitis
Polyarteritis nodosa Medium-sized to small Myalgia, arthralgia, fever, palpable purpura, skin ulceration or infarction, weight loss, testicular tenderness, neuropathy (involvement of vasa nervorum), hypertension, renal infarction
Hepatitis B associated
Kawasaki’s disease Medium-sized (coronary artery involvement) Children affected; desquamating rash over extremities, strawberry tongue
Large vessel vasculitis
Giant cell arteritis (temporal arteritis) Medium to large (temporal and ophthalmic arteries and their branches) Localised headache, systemic symptoms, tenderness temporal artery, jaw pain, visual loss—posterior ciliary artery (age ≥50 years)
Takayasu’s disease Large (aorta, brachial, carotid, ulnar and axillary arteries) Systemic symptoms, claudication, loss of pulses (typically Asian race ≤40 years)

GIT = gastrointestinal tract. SLE = systemic lupus erythematosus. PAN = polyarteritis nodosa. CNS = central nervous system.

* Frederich Wegener, German pathologist, described this in 1936.

Mikito Takayasu (1860–1938), Japanese professor of ophthalmology.

Soft-tissue rheumatism

This includes a number of common, painful conditions that arise in soft tissue, often around a joint. The problem may be general—for example, fibromyalgia; or restricted to a single anatomical region—for example, tendon, tenosynovium, enthesis or bursa. There are a large number of these conditions; the more common ones are described here.

Fibromyalgia syndrome

This syndrome is a common, frequently overlooked condition that mostly affects women in their 40s and 50s. It presents with a variable group of symptoms including widespread musculoskeletal aches and pains, and usually with symptoms of chronic fatigue. The musculoskeletal pain is mostly axial (neck and back) and diffuse. It is made worse by stress or cold. Pain may be felt ‘all over’ and is unresponsive to anti-inflammatory drug treatment. The combination of pain and fatigue may cause the patient severe disability. There is usually a poor sleep pattern. The patient wakes up not feeling refreshed, and more tired in the morning than later in the day. Note that no abnormal pathology has been found in the joints, muscles or tendons of these patients.

Rotator cuff syndrome

Supraspinatus tendinitis is the commonest form of rotator cuff syndrome. It is associated with degeneration and subsequent inflammation in the supraspinatus tendon as it is compressed between the acromion and humeral head when the arm is raised. It mostly affects 40- to 50-year-olds. Symptoms may begin following unaccustomed physical activities such as gardening.

Examination

Examine the shoulder joint. Note pain on abduction of the arm (Figure 9.67), with a painful arc of movement between 60 and 120 degrees of abduction. Involvement of other rotator cuff tendons causes similar painful movement. Biceps tendinitis is present in the majority of patients with a rotator cuff syndrome. Yergason’sy sign for biceps tendinitis is helpful (positive LR 2.8).10 The patient flexes the elbow to 90 degrees and pronates the wrist. The examiner holds the wrists and attempts to prevent the patient’s attempts to supinate the forearm. Inflammation of the head of the biceps causes pain in the shoulder since this muscle is the main supinator of the forearm.

Nerve entrapment syndromes

These are caused by compression of peripheral nerves at vulnerable sites and are associated with pain, paraesthesiae and numbness in a particular nerve distribution.

Meralgiaaa paraesthetica

Compression of the lateral cutaneous nerve of the thigh causes paraesthesiae and sensory loss over the lateral side of the thigh (page 375). This entirely sensory nerve passes through the lateral part of the inguinal ligament only just medial to the anterior superior iliac spine. Here it is subject to compression in patients who are obese, wear tight or heavy belts or spend long periods sitting. Diabetes, pregnancy and trauma can also be causes of problems with the nerve.

Morton’s ‘neuroma’

This is caused by compression of one or more of the interdigital plantar nerves by the transverse metatarsal ligament. Patients complain of a burning pain or ache that extends distally from the affected web space to the toes (most often the third and fourth).

Metatarsalgia is a non-localised ache that spreads across the forefoot involving the area of some or all of the metatarsal heads. It can occur in normal feet after prolonged standing but also occurs in a number of other foot conditions (Table 9.19), and is often associated with poor-fitting shoes. Morton’s metatarsalgia is interdigital nerve entrapment (usually between the third and fourth metatarsal bones. Patients describe burning pain between the metatarsal bones and may have numbness on the adjacent toes. They get relief by removing their shoes and massaging the foot.

TABLE 9.19 Causes of metatarsalgia

Tight or pointed shoes
Atrophy of metatarsal fat pad in elderly people
Plantar calluses
Metatarsophalangeal joint arthritis
Flat or cavus foot deformity
Overlapping toes
Interdigital entrapment
Hemiplegia
Peripheral vascular disease

References

1. Van den Hoogen H.M.M., Koes B.W., Van Eijk J.T.M., Bouter L.M. On the accuracy of history, physical, and the erythrocyte sedimentation rate in diagnosing low back pain in general practice: a criteria based review of the literature. Spine. 1995;20:318-327. Unfortunately, distinguishing mechanical from non-mechanical causes of low back pain such as ankylosing spondylitis is clinically difficult. However, tenderness to pressure over the anterior superior iliac spines and over the lower sacrum may, based on other studies, be somewhat helpful for the positive diagnosis of ankylosing spondylitis

2. Deyo R.A., Rainville J., Kent D.L. What can the history and physical examination tell us about low back pain? JAMA. 1992;268:760-765.

3. Fuchs H.A. Joint counts and physical measures. Rheum Dis Clin Nth Am. 1995;21:429-444. Describes useful quantitative methods to evaluate tenderness, pain on motion, swelling, deformity and limitation of movement

4. Katz J.N., Larson M.E., Sabra A., et al. The carpal syndrome: diagnostic utility of the history and physical examination findings. Ann Intern Med. 1990;112:321-327. This study compares the neurophysiological assessment of the carpal tunnel syndrome with the information obtained by examination and history. No single symptom or sign is sufficiently predictive

5. Glockner S.M. Shoulder pain: a diagnostic dilemma. Am Fam Phys. 51, 1995. 1677-1687, 1690-1692. Reviews the utility of symptoms and signs in differential diagnosis

6. Katz J.N., Dalgas M., Stucki G., et al. Degenerative lumbar spinal stenosis. Diagnostic value of the history and physical examination. Arth Rheum. 1995;38:1236-1241. Describes symptoms (severe lower limb pain which is absent when the patient is seated) and signs (including a wide-based gait, positive Romberg’s sign, thigh pain with lumbar extension) that help predict this rare condition in older patients

7. Murtagh J. Diagnosis of early osteoarthritis of the hip joint: the four-step stress test. Aust Fam Phys. 1990;19:389. Discusses the diagnosis of osteoarthritis of the hip in a systematic way, suggesting a four-step approach

8. Solomon D.H., Simel D.L., Bates D.W., et al. Does this patient have a torn meniscus or ligament of the knee? JAMA. 2001;286:1610-1620.

9. Scholten R.J., Opstetten W., vander Plas C.G., et al. Accuracy of physical diagnostic tests for assessing ruptures of the anterior cruciate ligament: a meta-analysis. J Fam Pract. 2003;52:689-694.

10. McGee S. Evidence-based clinical diagnosis, 2nd edn. Phildelphia: Saunders; 2007.

11. Grob J.J., Bonerandi J.J. Cutaneous manifestations associated with the presence of the lupus-anticoagulant. J Am Acad Dermatol. 1986;15:211-219. Antiphospholipid antibody syndrome can be associated with leg ulcers (that resemble pyoderma gangrenosum), livedo reticularis and fingertip ischaemia

12. Stevens G.L., Adelman H.M., Wallach P.M. Palpable purpura: an algorithmic approach. Am Fam Phys. 1995;52:1355-1362.

13. Elliott B.G. Finkelstein’s test: a descriptive error that can produce a false-positive. J Hand Surg Br. 1992;17:481-482. Careful explanation of the performance of this test (which is often misunderstood) appears in this article. Movement with the thumb folded into the hand can produce a false-positive result

a Maurice Raynaud (1834–1881) described this in his first work, published in Paris in 1862.

b Halushi Behçet (1889–1948), Turkish dermatologist.

c The traditional treatment, striking the lesion very hard with the family Bible, is not effective.

d Jean Martin Charcot (1825–1893), Parisian physician and neurologist. He became professor of nervous diseases, holding the first Chair of Neurology in the world. His pupils included Babinski, Marie and Freud.

e William Heberden (1710–1801), London physician, and doctor to George III and Samuel Johnson, described these in 1802. He was the first person to describe angina.

f Charles Jacques Bouchard (1837–1915), Parisian physician.

g Fritz de Quervain (1868–1940), professor of surgery in Berne, Switzerland.

h George Phalen, orthopaedic surgeon, the Cleveland Clinic.

i Jules Tinel (1879–1952), physician and neurologist in Paris. In 1915 he described tingling in the distribution of a nerve that had been severed and was regrowing when it was percussed.

j Alan Apley, orthopaedic surgeon, St Thomas’s Hospital, London.

k Hubert von Luschka (1820–75), professor of anatomy in Tübingen.

l Charles E Lasègue (1816–83), Professor of Medicine in Paris and pupil of Trousseau.

m Roman goddess of love—her ancient Greek equivalent was Aphrodite.

n Hugh Thomas (1834–91), ‘the father of orthopaedic surgery’, worked in Liverpool as a bone-setter but did not have a hospital appointment.

o Friedrich Trendelenburg (1844–1924), professor of surgery at Rostock, Bonn and Leipzig.

p Robert Osgood (1873–1956). He worked in France during the First World War and then at the Massachusetts General Hospital where he founded the X-ray department and subsequently developed several radiation-induced skin tumours.arl Schlatter (1864–1934), professor of surgery in Zurich. He pioneered a total gastrectomy operation in 1897.

q William Baker (1839–96), surgeon at St Bartholomew’s Hospital, London, described this in 1877.

r Thomas McMurray (1888–1949), the first professor of orthopaedic surgery in Liverpool.

s Hans Reiter (1881–1969), professor of hygiene in Berlin, described the syndrome in 1916. This was well before he became an enthusiastic Nazi.

t Thomas Morton (1835–1903), general and eye surgeon, Philadelphia Hospital, performed one of the first appendicectomies.

u Franklin Simmonds, orthopaedic surgeon, Rowley Bristow Hospital, Surrey, UK; he is now retired.

v Anthony Caplan, Welsh physician, described this in 1953.

w A syndesmosis is a joint where the bones are joined by fibrous ligaments or sheets.

x Lupus has been used as a name for any erosive disease of the skin; for example, lupus vulgaris is tuberculosis of the skin.

y Robert Mosley Yergason, American surgeon born in 1885, described this sign in 1931.

z Harry Finkelstein (1865–1939), surgeon, Hospital for Joint Diseases, New York.

aa The Greek word meros means thigh and algia means painful.